Burn Wounds
Over 1.5 million people suffer burns each year in the United States. More than 5,000 of these people will die as a direct result of the significant loss of the skin's integrity and subsequent bacterial invasion into the unprotected internal milieu of their bodies. Sepsis accounts for greater than 50% of the deaths related to patients who suffer from burns. Transmission of multi-resistant organisms to other patients, particularly in contained burn units, not only increases morbidity, but also adds an enormous cost to the healthcare system.
The current treatment of the burned patient involves fluid resuscitation, hemodynamic stabilization and the application of topical antimicrobials prior to wound excision and grafting. Bacteria flourish in dead tissue and intravenous antibiotics cannot penetrate this tissue because of its impaired blood supply. This necessitates the use of topical antimicrobials that are meant to curtail the systemic invasion of bacteria. Unfortunately, the commonly employed topical antimicrobials are often not enough to prevent the fatal consequences of burn wound sepsis. Synthetic antimicrobial peptides are specific proteins designed to encompass a greater spectrum of activity against bacteria (including multi-drug resistant organisms) and fungus than traditional topical agents.
Our proprietary peptide designs are extremely stable in hostile, non-physiologic environments. Alterations in the wound milieu, characteristics of burns, do not affect the potency or properties of the peptide making the designed peptides more effective and valuable to practitioners who manage burns, and infected or adversely colonized wounds. Sufficient promise was shown by several peptides through in vitro and in animal studies, to lead to the selection of one to be tested in several human clinical trials.
An initial double blind randomized, phase II/III clinical trial for the evaluation of a cream based peptide preparation in the topical treatment of burn wounds was conducted at Gandhi Medical College Hospital in Hyderabad, India in 2008. The mean duration to reach the total wound closure for peptide treated patients was found to be 8.4 days while the placebo group was 11.1 days. This was statistically significant at the (P<0.001). A second study consisting of 120 burn patients, begun in late 2008 was carried out at two hospitals in Hyderabad, India. In these studies the patients received no additional antibiotic therapy and none of the wounds were debrided. The final report indicated that there were no infections and significant accelerated healing with minimal scarring and the patients had significantly fewer hospital visits.
A final phase III study was recently completed utilizing a new cream composition combined with a very effective designed antimicrobial peptide. The results of this trial are found in this application.
Chronic Wounds
The loss of the skin's protective barrier as the result of unhealed wounds fosters the susceptibility to bacterial infection, invasion, and sepsis. About 40 million chronic wounds are treated globally annually. Those are wounds that get stuck in the inflammatory stage of wound healing and do not heal. Chronic wounds are the source of severe emotional and physical stress for patients and create a significant financial burden, both on patients and the whole healthcare system. In the chronic wound the balance between production and degradation of proteins is lost and degradation plays too large a role.
Chronic wounds present an enormous physical, social and economic burden worldwide and their incidence is on the rise with an aging population. It has been estimated that chronic wounds affect 120 per 100,000 people aged between 45 and 65 years and increases to 800 per 100,000 people aged over 75 year. Chronic wounds result from a number of different causes among them diabetes, pressure, atrial and venous insufficiency, vasculitis and burns. Additional complications, including infections, necrosis, tissue hypoxia, and exudates represent further challenges in dealing with a chronic wound. Poor nutrition, obesity, excessive alcohol consumption and smoking can then add an additional layer of complications to an already serious condition.
Normal wound healing progresses through three stages. The first is Inflammation that lasts 2 to 4 days from the time of injury. Upon injury hemostasis causes vascular constriction, and thrombus formation. Platelets in the wound release factors that recruit neutrophils and monocytes (macrophages), which in turn attract lymphocytes and fibroblasts to the site of injury. The proliferation stage overlaps the inflammatory stage, starts at about day 3 and lasts for several days. It is characterized by angiogenesis, collagen formation and epithelialization mediated by fibroblasts, and is complete when balance is achieved in collagen formation and its continuous breakdown by matrix metallo-proteases (MMPs). The Remodeling stage is the third and last stage and can extend over a year or more. Collagen remodeling continues, fibroblasts differentiate into myofibroblasts, vascularity decreases and tissue strength increases.
Bedsores, more properly known as pressure ulcers or decubitus ulcers, are lesions caused by many factors such as: unrelieved pressure; friction; humidity; shearing forces; temperature; age; continence and medication; to any part of the body, especially portions over bony or cartilaginous areas such as sacrum, elbows, knees, and ankles Although easily prevented and completely treatable if found early, bedsores are often fatal—even under the auspices of medical care—and are one of the leading iatrogenic causes of death reported in developed countries, second only to adverse drug reactions.
Results from a small trial utilizing a modified version of the burn cream are presented herein for the treatment of chronic wounds.
Cracked Heels
Cracked heels are a common foot problem and are often referred to as heel fissures. Cracked heels are commonly caused by dry skin (xerosis), and made more complicated if the skin around the rim of the heel is thick (callus). For most people this is a nuisance and a cosmetic problem but when the fissures or cracks are deep, they are painful to stand on and the skin can bleed—in severe cases this can become infected.
The skin is normally dry and may have a thick callus that appears as a yellow or dark brown discolored area of skin, especially along the inside border of the heel. Cracks in the skin are usually obvious.
If the cracks are severe enough, there will be pain upon weight bearing that is not there when weight is off the heel. The edges or rim around the heel will generally have a thicker area of skin (callus). Wearing open or thin-soled shoes usually make the symptoms worse.
Some people tend to have a naturally dry skin that predisposes them to the cracks. The thickened dry skin (callus) around the heel that is more likely to crack is often due to mechanical factors that increase pressures in that area.
Other factors that can be involved in the cause of cracked heels include:                prolonged standing (at work or home, especially on hard floors)        being overweight (this increases the pressure on the normal fat pad under the heel, causing it to expand sideways—if the skin is not supple and flexible, the pressures to ‘crack’ are high)        open back on the shoes (this allows the fat under the heel to expand sideways and increases the pressure to ‘crack’)        some medical conditions predispose to a drying skin (e.g. autonomic neuropathy in those with diabetes leads to less sweating; an underactive thyroid lowers the body's metabolic rate and there is a reduction in sweating, leading to a dryness of the skin)        skin conditions (e.g. psoriasis and eczema).        
Results from a small trial utilizing a modified version of the burn cream are presented herein for the treatment of cracked heels.